VERTIGO/DIZZINESS

     This is a common complaint in primary care medicine.  Vertigo refers to the sensation of movement, often a spinning sensation ,but a sensation of feeling pushed or pulled forwards, backwards or to a side or a tilting sensation may also be consistent with vertigo.  Vertigo occurs when the input from one of the paired labyrinths is interrupted resulting in unbalanced positional input from the contralateral labyrinth causing the sensation of movement.  Vertigo may be confused with either presyncope or the dysequilibrium syndrome.  Presyncopal patients feel light-headed or as if they are about to faint.  The work up in these patients should proceed as for a syncopal episode.  Dysequilibrium syndrome refers to a dizzy sensation or a pulling sensation while the patient is walking.  Symptoms decrease dramatically while the patient is seated.

     The first step in the work up of vertigo is to determine if the pathology is central (cerebellum and vestibular nuclei located at the pontomedullary junction in the brain stem) or peripheral (labyrinth and vestibular portion of the eighth cranial nerve).  Neighborhood signs are used to help distinguish a central from a peripheral origin of a patients vertigo.  Neighborhood signs which indicate a peripheral origin include tinnitis and hearing loss.  Central neighborhood signs include diplopia, cortical blindness, homonymous hemianopsia, dysarthria, dysphagia, drop attacks, extremity muscle weakness or sensory deficits, and unilateral or bilateral facial weakness or numbness.  Nystagmus is seen in most cases of vertigo.  Nystagmus associated with a peripheral origin is unidirectional, mixed, and is suppressed by fixation.  Unidirectional nystagmus refers to nystagmus in which the fast component always beats in the same direction.  Suppression by fixation refers to the fact that when the patient stares at an object the nystagmus ceases.  Mixed nystagmus has both a horizontal and a rotatory component.  In contrast, nystagmus associated with a central origin is multidirectional, pure and is not suppressed and in fact may be enhanced by fixation.  Multidirectional refers to a change in the fast component of the nystagmus as the patient changes their direction of gaze.  Pure means that the nystagmus is either horizontal or vertical or rotatory and does not exhibit a combination of these types of nystagmus.  Central nystagmus is never suppressed by fixation.  In difficult cases, electronystagmography can help differentiate between a central or peripheral origin.  Common causes of central vertigo include vertebrobasilar or cerebellar vascular insufficiency, multiple sclerosis, and migraine headache.  Some of the common etiologies of peripheral vertigo include benign paroxysmal positional vertigo, Meniere disease, neurolabyrinthitis, and perilymph fistula.

     There are multiple etiologies for vertigo but certain etiologies can be implied from the history or physical exam.  Benign paroxysmal positional vertigo should be suspected in patients who have vertigo associated with certain head movements, a brief latency to the onset of vertigo and fatigability with repeated positioning of the head.  This can be demonstrated by performing the Dix-Hallpike maneuver and may be treated with the Epley maneuver.  Vertigo which develops after recent head trauma may be due to a perilymph fistula and these patients should be referred to an ENT specialist for pneumatic otoscopy which establishes the diagnosis.  Meniere’s disease is characterized by repeated attacks of vertigo with associated tinnitus, hearing loss, nauseas and vomiting.  Attacks may last for hours or days.  When associated with headache, migraine is a possible etiology.  Multiple sclerosis should be suspected when there are associated neurologic deficits.

     The work up should include a complete neurologic exam along with the Dix-Hallpike maneuver.  Patients with neurologic deficits should undergo further evaluation with an MRI scan of the brain.  Patients with a normal neurologic exam and persistent symptoms of vertigo should be considered for further testing with an audiogram and either electronystagmography (ENG) or brain-stem auditory evoked responses (BAERs).  If these screening tests are normal no further work up is needed.  If the screening tests are abnormal, then imaging of the posterior fossa and cerebellopontine angle with an MRI scan should be performed.  Also, patients with a history of risk factors (hypertension, diabetes mellitus, hypercholesterolemia, tobacco abuse history, or a positive family history) for peripheral vascular disease should undergo brain MRI scanning to rule out brain-stem or cerebellar hemorrhage or infarcts.

     Therapy directed at the underlying etiology may resolve symptoms of vertigo.  When vertigo is secondary to acute or recurrent peripheral vestibulopathy, medication may help alleviate symptoms.  Meclizine HCl (12.5-25 mg Q 6 hours) with or without a benzodiazepine (oxazepam 10-15 mg Q 6 hours) is often effective; however, meclizine is not effective when used to treat vertigo of other etiologies.  Since drowsiness is a common side effect of both of these medications, methylphenidate HCl (5 mg at morning and noon) may be added to combat sedation.